Behavioral genetic methodologies from twin and adoption studies through DNA analysis will be described and applied to address longstanding questions about the origins of individual differences in behavioral traits.

Reviews

MF

Matt is absolutely fantastic at teaching- he is very engaging and great at explaining things and the course itself is fascinating. Thank you to Matt and Bridget!

NS

Sep 01, 2019

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I loved this course because it made me think about topics and points that I had never considered before, and I think it's a really fascinating area of genetics.

From the lesson

7

I am sure many of you wondered about the impact of age on biometric estimates when we discussed general cognitive ability last week. Indeed some of you asked about this issue on the Forums. You were right to raise the question because this is an important issue in the behavioral genetic literature. Given its importance, I thought it might work best to place the question of age moderation in a larger context, which we do this week. We will begin the week by returning to the distinction between shared and non-shared environmental influences, an important distinction in the behavioral genetic literature. You will see that while shared environmental influences are not important for most behavioral phenotypes, there are a few exceptions (including general cognitive ability). However, in all of these exceptional cases, the magnitude of shared environmental influences decreases with age as the heritability increases.

To understand this developmental pattern, at least from a behavioral genetic perspective, it is helpful to consider mechanisms of gene-environment correlation as well as behavioral genetic perspectives on family socialization. We end this unit with an overview of behavioral genetic research on aging.

Taught By

Matt McGue

Transcript

Okay, welcome back. The fourth module in the seventh unit. We're in the seventh unit. Uh,were really talking about the environment and development, and last time I introduced the notion of GE correlation, gene environment correlation and I said it had three very important Implications for psychology and behavioral genetics. Two of which I went through last time. The third of which I'm going to go through today. One is that the existence of GE correlation really requires that we broaden our perspective of what we mean by genetic. What we mean by heritable when we're talking about behavior that in part, heritable effects and behavior might be mediated by the environments, the experiences that we choose. Or the reactions or behaviors illicit from others. Secondly, GE correlation is important in helping us understand the developmental pattern that emerges from behavioral genetic research. Heritability increases, shared environment influences decrease. The third thing I said that I'd come back to, that's what I'm going to do in this module is talk about how GE correlation is important for us to understand parent offspring resemblance. So, parent behavior is related to a wide variety of offspring phenotypes. In, and here what I've done is I guess I have five different examples here. But there I, I, there are hundreds, thousands of these. Um,it took me about five minutes to pick these out of the literature the recent literature. Parents who did well in school tend to have children who also do well in school. Parents who smoke, the children of parents who smoke have an excess risk of smoking. Children of overweight parents are more likely to be obese. Children of professional parents are more likely to have large vocabularies. And anxious parent, anxious children, I'm sorry, tend to have parents who are overprotective. There are thousands of studies in Psychology showing relationship between certain parent factors or behaviors and the functioning of the children that they're rearing. But a question that I think unfortunately is not often asked about these associations, is whether or not they are really casual. Often we just assume they're causal. Maybe you don't do that, but I think a lot of times, let's say in the, in the, in the mass media, you'll see a study reporting relationship between obesity in parents and children and the presumption is that somehow the environment the parents created lead their children to share this trait of obesity. That might be the case, but I think we need to look at it more closely have, having gone through this course in behavioral genetics. And let me just take an ex, example of one of those studies. And I don't really know why a, anxious children have overprotective parents. It may be that if you're overprotective as a parent, you tend to produce children who are anxious. That's certainly a possibility. And it certainly needs to be explored. But just observing the correlation between over-protectiveness in the parent and anxiety in the children. Doesn't establish that this is causing that. And it doesn't establish it. In large part because of GE correlation.That is maybe. Parents who are overprotective are anxious. That is, if I'm a parent and I'm anxious, maybe one way I express my anxiety is try to protect the children I rear. I don't know if that's true, but it's not an absurd conjecture to imagine that parents who are overprotective Are overprotective because they're anxious. So, this observation here that overprotective parents have anxious kids may be nothing more than anxious parents have anxious kids, and if anxious parents have anxious kids, well, one mechanism by which they might have anxious kids is genetics. This that is that there ang anxiety is inheritable it we haven't gone through that in this course but I'm sure at this point that you can imagine that there is plenty of evidence that suggests that it is partially heritable so that their are genes that underlie anxiety in parents there are genes that underlie anxiety in children. And that parents are transmitting that gene. So maybe over protective isn't a cause of anxiety in their children but rather just correlated with the genes that lead to anxiety in the children. A GE correlation, and in fact, a passive GE correlation. So yes. Being over protective maybe does cause anxiety in the children, but it might also arise that correlation because of passive GE correlational events. I'm sure some of you are also thinking, well sure, it might also arise because of reactive GE correlational effects. That is, if I have a child who is timid and anxious. Maybe the way I react to that, as a parent, is to try to protect him or her. So my over-protectiveness isn't really shaping the anxiety of my child, but rather, a reflection, a reaction to that. So, we know that overprotective parents is correlated with anxiety in the children. That may be because over-protectiveness causes anxiety, it may be because over-protectiveness is correlated with the genes for anxiety, a passive GE correlational effect, or maybe anxiety in the children elicits over-protectiveness in the parent. There are many possibilities that need to be explored here. We can't draw causal influences, inferences just from observing the correlation. It turns out that behavioral genetic methodology can help us begin to try to sort things out here, and I'm going to try to illustrate this with another phenotype. Smoking during pregnancy. Something, of course, that's not to be recommended. It's not to be recommended because there's incontrovertible evidence from experimental studies on animals, mostly rodents, that shows that pregnant smoking during pregnancy Leads to all sorts of physical problems in the fetus. Not as if every fetus has the problem. But it elevates the risk for these. It elevates the risk for miscarriage, low birth weight, prematurity. Primarily because it lowers the distribution of oxygen to the developing fetus. So, we know from experimental studies in animals that maternal smoking leads to physical problems and mostly those problems are associated with lack of oxygen leading to low birth weight and prematurity. Epidemiological research in humans has shown that there's a correlation between maternal smoking and ADHD, Attention Deficit Hyperactivity Disorder. And I'm going to illustrate that this is a very robust association. I don't think anybody questions the existence of this association. What I want to, try to raise the question here today is, is it a causal association? And we use two large recent studies to illustrate this. One study is from Finland, the other from Sweden. So I guess they're biased in the sense they're both coming from Scandinavian countries. But the Scandinavian countries have those great databases that researchers can use. The Finnish study involves almost 900,000 children. The Swedish study, almost 800,000. These are massive sample sizes. And in both cases - I'm not going to go through the particular research design - but in both cases, they have very good information upon, about maternal smoking, because in both these countries Mothers get excellent care while pregnant, so they can carefully document maternal smoking, I'm sure there's some under reporting of that, but there's also quite a bit of reporting of smoking as well. And they can follow these children up through the registry system to see if they develop ADHD. In this first graph, what I'm reporting here. I've taken the data out of these two studies, and just put it in a graph here. Reporting the association between maternal smoking and risk of ADHD, and the way things are reported in the study, this is the Swedish sample. And the Swedish sample, they divided up the mothers as either moderate smokers or heavy smokers. Depending upon how many cigarettes you smoke in a day during pregnancy. In the Finnish sample, I just have for all mothers smoking, all smoking mothers. And the way the reporting results is basically the ratio of the risk of having ADHD if your mother is a smoker Versus if you don't have a smoking mother. So, if there's no effect, then the, the ratio here would be one, so I've highlighted that. And what you see is, if you have a mother that smokes, you basically double your risk of ADHD, a little more if you have a heavy smoking mother than a moderate smoker. Where here it's 1.6, here it's two. But it's basically, it's very consistent data across the two Scandinavian studies. Mothers who smoke, their children have about twice the risk of ADHD compared to mothers who don't smoke. It's a causal. But maybe it isn't causal. And, and certainly, we know, maternal smoking is not good for the developing fetus. We know that from the animal studies. But maybe, mothers who smoke, maybe that's actually associated with other factors that might lead to ADHD. Maybe mothers who smoke are more likely to be poor. And maybe it's the poor environment that they're growing up in that leads to ADHD. Or maybe mothers who smoke, they smoke because, we know for example, that people with ADHD are increased risk of being a smoker. Nicotine is a psychoactive substance. It's a stimulant. In part, and people with ADHD is more likely to use this particular stimulant than people not with ADHD. So many those smoking mothers actually had ADHD earlier in their life, and they're transmitting risk to their children, not because they're smoking while pregnant, but because they carry genes that might increase risk for ADHD. How can we begin to look at this? One way to begin to look at this question is to use what's called the within sibship design. So we take the mother, who was smoking. And she has her first baby, and she smoked while she was pregnant. But between the time she had her first baby In the second baby she stopped smoking. Maybe because of affective health interventions. Or conversely it could be that the first baby she didn't smoke but the second baby she did smoke. But in any case, in those large Scandinavian samples there are quite a few times where a mother had a baby Where she was smoking and another time, a sibling of that baby where she didn't smoke. So you have two babies, one whose not exposed to maternal smoking, the other who is, but having the same mother. If smoking while pregnant is caus, we know it's causal pf physical developmental problems, but is it causal of ADHD. If it's causal of ADHD right, this baby should have a higher risk than that baby. That's the prediction. If maternal smoking is causal, this baby should have a higher risk than that baby. If it isn't causal, then the two babies should have similar level of risk. What do you find in these studies? Well the data are actually extremely consistent across the two studies, these two very large studies. In the red bars here, now I'm comparing not babies of smoking mothers versus babies of non-smoking mothers. Overall, But just babies of smoking mothers to their siblings when the mother was not smoking. In this case, within the shibship, there's no effect of maternal smoking. That is, the mother who smoked when she had a child, when she did smoke while pregnant And she had a child while she didn't smoke while pregnant. There was no difference in the risk of ADHD to those two children. Smoking did not appear...does not appear does not appear to be a causal influence on risk to ADHD because you don't get the within sibship effect. Why is it associated then overall? It's associated overall because there are other factors that may be...must be correlated with maternal smoking that are really the causes here of ADHD risk. What might those be? I mentioned those in the previous slide. Those might have to do with the The home environment or it might have to do with genetic factors, but maternal smoking per se does not appear to be causal because you don't get the within-family effect. So, parental behavior is related to offspring functioning. But what a behavioral geneticist will want to emphasize is the mere observation of a correlation between parent behavior and offspring functioning doesn't isn't the basis of some causal inference. That could be for genetic reasons, it could be for environmental reasons. We don't know just be observing the correlation. You're going to, you shouldn't allow me, if somebody reported a study that said, highly religious parents tend to have highly religious children, and I came along and said, oh, there's a parent-offspring correlation in religiousness, that must be genetic, I would hope that you would challenge me. Because that correlation by itself can't be the basis for a strong causal conclusion. What I'm arguing at the same time is, if I observe a correlation between parent religiousness and offspring religiousness, I'm not going to let you say that that necessarily is environmental either. You need more evidence. Where that additional evidence is going to come from often from behavioral genetic studies, like the within sibship study I gave you previously in this module. So that ends this fourth module. Next time, I'm going to take up gene-environment interaction, something that we talked about much earlier in the course, but it's such an important concept, I want to take it up again. Thank you.

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